The crucial role of inflammation in the pathogenesis and clinical outcomes of cardiovascular disease (CVD) has recently gained increased attention. In particular, residual inflammation, measured with high-sensitivity C-reactive protein (hsCRP) remains strongly predictive of recurrent events, even in statin-treated patients. Similarly, elevated hsCRP in apparently healthy individuals identifies a higher-risk group in whom statin therapy significantly reduces the risk of first major CVD events even if LDL-cholesterol is normal. This report provides an updated understanding of the role of chronic, low-grade inflammation in CVD and highlights new seminal research findings, especially in atherosclerosis, myocardial infarction, heart failure, and pericarditis. Consensus recommendations are summarized for screening, evaluation, and CVD risk assessment; inflammatory biomarkers in cardiovascular imaging; inflammation inhibition in behavioral and lifestyle risks; and anti-inflammatory approaches in primary and secondary prevention as well as in heart failure and other CVDs. This report also addresses current challenges and future opportunities. For example, it cautions that not all trials of anti-inflammatory therapy in secondary prevention have been successful and such trial evidence is needed before broad recommendations for other agents can be made. Additionally, in successful trials, the interplay between inflammation and key physiological systems often remains incompletely examined. Another promising area of research is the role that novel special pro-resolving bioactive lipid molecules play in promoting the resolution of inflammation and CVD risk reduction. In aggregate, the evidence linking inflammation with atherosclerotic CVD is no longer exploratory but is compelling and clinically actionable. The time for taking action has now arrived.
“Despite advances such as interleukin‑6–targeted therapies, implementation remains limited, as clinicians are unlikely to treat what they do not routinely measure. Addressing current gaps in inflammatory risk assessment presents both a challenge and an opportunity to better personalize CVD prevent...”
Mensah et al. (2025) studied this question.